Product Usage
MOTS-C 10mg IS INTENDED AS A RESEARCH CHEMICAL ONLY. This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. All product information available on this website is for educational purposes only. Bodily introduction of any kind into humans or animals is strictly forbidden by law. This product should only be handled by licensed, qualified professionals. This product is not a drug, food, or cosmetic and may not be misbranded, misused or mislabled as a drug, food or cosmetic.
MOTS-c is a 16 amino acid peptide that’s encoded in mitochondrial DNA (mt-DNA). It’s involved in a number of cellular functions, including:
- Energy metabolism: MOTS-c regulates the Folate-AICAR-AMPK pathway.
- Insulin resistance: MOTS-c can improve physical function in mice of all ages.
- Inflammatory response: MOTS-c inhibits ROS production.
- Cardiovascular disease: MOTS-c can protect against cardiac dysfunction and pathological remodeling.
MOTS-c is expressed in response to exercise and stress. It’s also believed to play a role in promoting healthy aging.Here are some other effects of MOTS-c:
- Skeletal muscle metabolism: MOTS-c regulates skeletal muscle metabolism.
- Gene expression: MOTS-c regulates gene expression.
- Obesity: MOTS-c can improve obesity.
- Osteoporosis: MOTS-c may have beneficial effects on osteoporosis.
- Postmenopausal obesity: MOTS-c may have beneficial effects on postmenopausal obesity.
- Alzheimer: MOTS-c may have beneficial effects on Alzheimer.
MOTS-c levels decline with age. Synthetic biology technology may be used to introduce MOTS-c into probiotics to achieve its accurate and controllable expression. - Skeletal muscle metabolism: MOTS-c regulates skeletal muscle metabolism.
10mg/ml solution provided in a 4ml vial.
Clinical Research
“The Mitochondrial-Derived Peptide MOTS-c Promotes Metabolic Homeostasis and Reduces Obesity and Insulin Resistance Mitochondria are known to be functional organelles, but their role as a signaling unit is increasingly being appreciated.
The identification of a short open reading frame (sORF) in the mitochondrial DNA (mtDNA) that encodes a signaling peptide, humanin, suggests the possible existence of additional sORFs in the mtDNA. Here we report a sORF within the mitochondrial 125 RNA encoding a 16-amino-acid peptide named MOTS-c (mitochondrial open reading frame of the 12S rRNA-c) homeostasis. Its primary target organ appears to be the skeletal muscle, and its cellular actions inhibit the folate cycle and its tethered de novo purine biosynthesis, leading to AMPK activation. MOTS-c treatment in mice prevented age-dependent and high-fat-diet-induced insulin resistance, as well as diet-induced obesity.
These results suggest that I mitochondria may actively regulate metabolic homeostasis at the cellular and organismal level via peptides encoded within their genome. that regulates insulin sensitivity and metabolic Lee, Changhan & Zeng, Jennifer & G. Drew, Brian & Sallam, Tamer & Martin-Montalvo, Alejandro & Wan, Junxiang & Kim, Su-Jeong & Mehta, Hemal & Hevener, Andrea & Cabo, Rafael & Cohen, Pinchas. (2015). The Mitochondrial-Derived Peptide MOTS-c Promotes Metabolic Homeostasis and Keduces Obesity and Insulin Kesistance. Cell metabolism. 21. 443-494.”
The identification of a short open reading frame (sORF) in the mitochondrial DNA (mtDNA) that encodes a signaling peptide, humanin, suggests the possible existence of additional sORFs in the mtDNA. Here we report a sORF within the mitochondrial 125 RNA encoding a 16-amino-acid peptide named MOTS-c (mitochondrial open reading frame of the 12S rRNA-c) homeostasis. Its primary target organ appears to be the skeletal muscle, and its cellular actions inhibit the folate cycle and its tethered de novo purine biosynthesis, leading to AMPK activation. MOTS-c treatment in mice prevented age-dependent and high-fat-diet-induced insulin resistance, as well as diet-induced obesity.
These results suggest that I mitochondria may actively regulate metabolic homeostasis at the cellular and organismal level via peptides encoded within their genome. that regulates insulin sensitivity and metabolic Lee, Changhan & Zeng, Jennifer & G. Drew, Brian & Sallam, Tamer & Martin-Montalvo, Alejandro & Wan, Junxiang & Kim, Su-Jeong & Mehta, Hemal & Hevener, Andrea & Cabo, Rafael & Cohen, Pinchas. (2015). The Mitochondrial-Derived Peptide MOTS-c Promotes Metabolic Homeostasis and Keduces Obesity and Insulin Kesistance. Cell metabolism. 21. 443-494.”
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